Enhancement of arm exercise endurance with dihydroxyacetone and pyruvate R. T. STANKO, R. J. ROBERTSON, R. J. SPINA, K. D. GREENAWALT, AND F. L. GOSS

capacity

J. J. REILLY,

JR.,

Department of Medicine, Montefiore Hospital, Program of Health and Physical Education, and Department of Surgery, Presbyterian- University Hospital, University of Pittsburgh, Pittsburgh, Pennsylvania 15213

STANKO, R.T.,R.J. ROBERTSON, R.J. SPINA, J.J. REILLY, K. D. GREENAWALT, AND F. L. Goss. Enhancement of arm exercise endurance capacity with dihydroxyacetone and JR.,

DHAP is simply substituted for other CHO in the diet. However, it is not known whether dietary supplementation of DHAP will augment intramuscular glycogen and improve endurance capacity in humans. As such, it was the purpose of this investigation to determine the effect of dietary DHAP supplementation on muscle glycogen content and submaximal arm endurance capacity in human subjects. Muscle extraction of glucose from blood is an important determinant of CHO metabolism and submaximal endurance capacity (3, 4). In rats, during exercise, hepatic glycogenolysis and glucose release are related to hepatic glycogen content (22). Unpublished observations in rats in our laboratory suggest that DHAP feeding will increase hepatic glycogen content. This may, in turn, augment hepatic glucose release and blood-borne glucose pools. However, it has not been determined if the inclusion of DHAP in a standard diet augments blood-borne glucose pools and/or increases muscle glucose extraction in humans, thereby forestalling physiological fatigue during prolonged exercise. The present investigation examined this question.

pyruvate. J. Appl. Physiol. 68(l): 119-124, 1990.-The effects of dietary supplementationof dihydroxyacetone and pyruvate (DHAP) on endurancecapacity and metabolic responsesduring arm exercise were determined in 10 untrained males (20-26 yr). Subjectsperformed arm ergometer exercise (60% peak O2 consumption) to exhaustion after consumption of standard diets (55% carbohydrate, 15% protein, 30% fat; 35 kcal/kg) containing either 100 g of Polycose(placebo,P) or DHAP (3:1, treatment) substituted for a portion of carbohydrate. The two diets were administered in a random order, and each was consumedfor a 7-day period. Biopsy of the triceps musclewas obtained immediately before and after exercise.Blood samples were drawn through radial artery and axillary vein catheters at rest, after 60 min of exercise,and at exercisetermination. Arm endurancewas 133 * 20 min after P and 160 $- 22 min after DHAP (P c 0.01). Triceps glycogenat rest was 88 t 8 (P) and 130 t 19 mmolfkg (DHAP) (P c 0.05). Whole arm arteriovenous glucosedifference (mmol/l) was greater (P c 0.05) for DHAP than P at rest (0.60 t 0.12 vs. 0.05 + 0.09) and after 60 min of exercise (1.00 + 0.12 vs. 0.36 t O.ll), but it did not differ at exhaustion. Neither respiratory exchange ratio nor respiratory quotient differed betweentrials at rest, after 60 min of exercise,or at exhaustion. Plasma free fatty acid, glycerol, METHODS ,&hydroxybutyrate, catecholamines,and insulin were similar during rest and exercise for both diets. Feeding DHAP for 7 Subjects. Ten physically active male university studays increasedarm muscleglucoseextraction before and during dents participated as subjects. On average, they were 23.3 exercise,thereby enhancingsubmaximalarm endurancecapac- + 0.8 (SE) yr old, weighed 81.6 (SE) kg, and had a peak ity. 62, consumption (VO2 peak)on an arm ergometer of 27.9 t 1.2 (SE) ml*kg-l*min-l. All experimental procedures arm endurance were approved by the University of Pittsburgh’s InstiCARBOHYDRATE (CHO) supplementation increases muscle glycogen concentration and improves exDIETARY

ercise endurance capacity in humans (2, 13, 20). It has recently been shown that the addition of the CHO metabolites dihydroxyacetone and pyruvate (DHAP) to the diet of the rat over a ll%day period increases the percent of carcass glycogen (21). Because CHO depletion is frequently associated with fatigue during prolonged submaximal exercise the addition of DHAP to the normal daily diet of humans may have ergogenic application. With this ergogenic procedure, the percent of kilocalories derived from CHO, fat, and protein is not different from that of a balanced daily diet. An isocaloric amount of 0161-7567/90

$1.50 Copyright

tutional Review Board for Human Subjects Experimentation. Subjects were informed of the possible side effects of the experiment and gave their written consent to participate. Experimental design. A double-blind design was used with each subject randomly assigned to one of two dietary combinations. The order of the treatment and placebo diets within the combinations was presented in a crossover configuration. Both diets provided 35 kcal/kg body wt and had a composition of 55% CHO, 30% fat, and 15% protein. The composition of the diets was similar to the subjects’ normal daily food intake as determined by a T-day dietary recall. The treatment diet (DHAP) contained 75 g of dihydroxyacetone and 25 g of sodium pyruvate. DHAP were added to Jello Instant Pudding,

0 1990 the American

Physiological

Society

119

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which was ingested during three daily meals. Sugar-free fiber was added to the pudding to promote congealment. DHAP (Chemical Dynamics, South Plainfield, NJ) accounted for 7% of the total kilocalories on days 1 and 2 and 15% of the kilocalories on days 3 through 7. This percent was chosen because previous studies in rats indicated that carcass glycogen increased when DHAP represented 15% of the total kilocalories in the normal daily diet. However, total consumption of DHAP did not exceed 400 kcal in a given 24-h period. This combination was chosen because preliminary studies in rats evaluating the effect of a group of CHO metabolites on hepatic glycogen content showed that DHAP consistently increased hepatic glycogen by twofold. At the time of this experiment, sodium pyruvate was the only form of pyruvate available for human consumption. To avoid excess Na’ intake, maximum consumption of sodium pyruvate was set at 25 g, necessitating a 3:l mixture of DHAP. The placebo diet contained an isocaloric amount of Polycase, which was substituted in the pudding for DHAP. The Na+ content of both diets was made equivalent by addition of sodium citrate to the placebo diet. Both the treatment and placebo diets were administered at the University of Pittsburgh’s Clinical Research Center. Randomization of the diets was performed by the Center’s chief clinical dietitian. The subjects and all personnel associated with exercise testing were unaware of the order of randomization of the diets. The first diet was consumed over a 7-day period. Immediately after completion of the first diet, arm exercise was performed to determine submaximal endurance capacity. The second diet was consumed for a 7-day period beginning 714 days after completing the first experimental trial. Arm endurance capacity was again determined. The subjects were instructed to avoid alcohol and prolonged exhaustive exercise during the feeding periods. Exercise testing. During preliminary testing and the experimental trials, subjects were seated on a cycle ergometer with the legs extended over a support bar to standardize lower body leverage. The hips and shoulders were harnessed to a stabilizing backboard to decrease trunk movement and to regionalize exercise to the muscles of the arms and shoulders. To familiarize subjects with the testing protocol, exercise with the arm ergometer and torso-stabilizing procedure was undertaken during a preexperimental screening period. A Monark 881 arm ergometer was positioned on a platform directly in front of the subject and adjusted such that the crank axle was at shoulder level and the elbow was extended but not locked when the handgrip was farthest from the body. The crank rate (50 rpm) was regulated by an electronic metronome. The ergometer was calibrated before each trial throughout the experiment. All exercise tests were terminated at the point of exhaustion, which was defined as the inability to maintain a crank rate of 50 rpm for 15 consecutive s. Subjects were regularly instructed to maintain the approximate crank rate and to continue exercise as long as possible. Forceful verbal motivation was not used. The termination criterion was verified by two independent observers. Ambient temperature and relative humidity were 2O-22°C and 50%,

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respectively, during all testing conditions. All tests were started at 0900 h with subjects in a lo- to 12-h postabsorptive state. Subjects exercised continuously except for a 90-s rest period every 60 min during which time blood samples were obtained and blood flow measurements were performed. Before the experimental trials, v02peak was determined during arm exercise. The initial power output on the arm ergometer was 24.5 W and was incremented by 24.5 W every 3 min. This test established the power output equivalent of 60% vogpeak that was used in the experimental trials. Oxygen consumption (Vo2) was measured every minute of exercise with the peak value determined when VOW leveled off in the presence of increasing power output. In all tests of VO 2pe&respiratory exchange ratio (R) exceeded 1.1. During the experimental trials, arm exercise was undertaken at a power output equivalent to 60% v02peak. Both arm endurance trials were terminated at the point of exhaustion according to the criterion described previously. The 60% relative metabolic rate was chosen because it was determined during pilot experiments that this exercise intensity could be sustained for extended periods of time. Consistency of vo2 over time was verified every 10 min of exercise. v02 did not. differ between trials and was consistently equal to 60% Vozpe& over the time course of both exercise performances. Blood chemistry variables. A 20.3-cm Erythrocath was inserted through an antecubital vein until the tip was near the axillary vein. This enabled sampling of venous blood drainage for the whole arm. A catheter was also placed in the radial artery of the opposite arm. Both catheters were secured with tape, and patency was maintained with saline flush every 60 min. Blood samples were drawn every 60 min of exercise. Arterial blood was analyzed for pH, CO2 (ml/dl), 02 (ml/dl), lactate (mmol/ 1)) pyruvate (mmol/l) , bicarbonate (meq/l) , glucose (mmol/l), free fatty acids (mg/l), glycerol (pmol/ml), and /3-hydroxybutyrate (pmol/ml). Venous blood was analyzed for the same variables as well as epinephrine (pg/ ml), norepinephrine (pg/ml), and insulin (pU/ml). Respiratory quotient (RQ) was determined for the whole arm by using blood gases. Glucose extraction was calculated as the difference between arterial and venous glucose concentrations. Fractional extraction of glucose was calculated as arteriovenous glucose difference divided by arterial glucose concentration. O2 and COZ content of whole blood were calculated according to the following equations (9, 16) 0 2 = 02 (saturation)

X 1.390

co 2 = CO2 (plasma) CO2 plasma

X Hb + 0.003 X Poe

X [LO -

(ICI X Kz X I&)]

= 2.226 x 0.0307 x Pco2 x [l.O + 10.0 (pH - pK)]

K 1 = 0.0288 Hb (g/100 ml) K 2=

KS =

1 2.244 - 0.422 (02 saturation) 1

8.74 - pH

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EXERCISE

AND DIHYDROXYACETONE

Glucose (12), lactate (ll), pyruvate (ll), glycerol (23), and P-hydroxybutyrate (24) were analyzed in duplicate in whole blood by enzymatic techniques. Plasma insulin was determined by radioimmunoassay (19). Plasma catecholamines were determined by high-performance liquid chromatography with electrochemical detection (10) modified for plasma (Plasma Catecholamines: LC/EC Application, Bioanalytical Systems, West Lafayette, IN). Plasma free fatty acids were determined by enzymatic techniques (NEFAC, Wako Pure Chemical, Osaka, Japan). O2 saturation was measured spectrophotometritally (8). 2MuscZeglycogen. Before exercise and at exhaustion, a lo-mg biopsy of the triceps muscle was obtained with a Tru-cut biopsy needle. For each biopsy, a 5-mm incision was made in the skin after 0.5-1.0 ml xylocaine was injected subcutaneously to induce local anesthesia. Biopsy samples were immediately frozen in liquid Nz, stored at -lO”C, and later analyzed for glycogen by alkaline extraction, ethanol precipitation, and acid hydrolysis (mmol/kg wet wt) (17). Blood flow. Blood flow in the whole arm was measured by bioelectrical impedance in 4 of the 10 subjects (18). Impedance was measured with a Minnesota Impedance Cardiograph (Surcom, Minneapolis, MN) with electrodes applied to the arm at axilla and wrist by means of 2.5cm tape around the circumference of the arm. Impedance recordings were made for 30 s before and 30 s during the intermittent rest periods of each exercise trial. Blood flow was calculated according to the following equation

AV = P x (L/&J2 x dz/dt x T where AV is blood volume of each pulse (ml), P is resistivity of blood w x cm), L is distan ,ce between sensing electrodes (cm), 20 is base-line impedance (a), dz/dt iS maximal rate of change of impedance (Q/s), and T is ventricular ejection time (s). Cardiorespirutory measures. Heart rate was measured every 20 min during exercise by using the R-R intervals on an electrocardiogram. Respiratory-metabolic responses were determined by standard techniques of open circuit spirometry. Inspired ventilation was measured with a Parkinson-Cowan (CD-4) gasometer. The concentrations of CO2 and 02 in expired air were measured with a Beckman LB-2 COZ analyzer and an Applied Electrochemistry S-3A analyzer. The analyzers and gasometer were integrated into a laboratory computer (Apple IIe). R, iToZ, and COz production were determined every 10 min of exercise. The analyzers were regularly calibrated by using previously standardized gases. The dry gasometer was calibrated against a Tissot spirometer. Statistical analysis. Differences in endurance capacity between experimental trials were analyzed with the paired t test (7). Changes in blood chemistry, muscle glycogen, and cardiorespiratory responses within and between dietary conditions were examined by using a two-way analysis of variance (condition X time) with repeated measures on both factors. Significant main effects and interactions were evaluated with the Scheffi! post hoc test (15). Responses were not affected by order of treatment.

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RESULTS

Submaximal endurance capacity during arm exercise increased (P < 0.01) from 133 t 20 min during the placebo trial to 160 t 20 min during the treatment trial (Table 1). Resting muscle glycogen (Fig. 1) concentration was greater (P < 0.05) after consumption of the treatment (130 t 19 mmol/kg) than placebo (88 t 8 mmol/ kg) diet. Muscle glycogen concentration decreased during exercise and did not differ between experimental trials at the poin t of exhaustion. Arterial and venous glucose concentrations are presented in Table 2. Arterial and venous glucose concentrations before exercise, after 60 min of exercise, and at exercise termination were not different between trials. Arteriovenous glucose difference was greater (P c 0.05) before exercise and after 60 min of exercise during the TABLE 1. V&peak3 treatment sequence, and endurance capacity of subjects performing prolonged arm exercise Subj No.

8 9 10

ml-l.

vo

Endurance Capacity After P, min

Treatment Sequence

2 peak,

kg-l.min-’

P:T P:T T:P

21.0 28.4 25.6 28.2 22.4 32.0 28.6 29.2 30.4 33.1

78

T:P

T:P P:T T:P P:T T:P P:T

27.921‘2 Tjogwak,peak 02 consumption; * P < 6.01 vs. P.

Endurance Capacity After T, min

Mean & SE

136 138 271 175 48 174 121 89 103

101 196 179 318 193 61 160 128 118 147

133t20

160&22*

P, placebo diet; T, treatment diet.

1a

TREATMENT

1

EXHAUSTION “pO.05

(n denotes

vs placebo n=lO number of subjects)

FIG. 1. Glycogen concentration of triceps muscle before and after exhaustive arm exercise in subjects consuming glucose polymer (placebo) or dihydroxyacetone and pyruvate (treatment) for 1 wk. Values are means k SE.

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122 TABLE

EXERCISE

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2. Glucose concentrations Rest

TABLE 3. Lactate and pyruvate Exhaustion

60 min

Arterial Placebo 4.24-cO.10 4.llzkO.19 4.25t0.17 Treatment 4.64k0.29 4.34k0.21 4*10-c-0.14 Venous Placebo 4.05t0.23 3.87kO.16 3.59-r-o. 15 Treatment 4.04kO.35 3.34kO.15 3.13t0.21 Arteriovenous Placebo 0.05+0.09 0.36t0.11 0.66,tO.lO Treatment 0.60t0.13* 1.00zk0.12* 0.97kO.13 Values are means + SE in mmol/l; n = 10 at all intervals of evaluation. * P < 0.05 vs. placebo.

q

AND PYRUVATE

Rest .

Arterial

60 min

Exhaustion

1.362t,O.210 1.38420.131

2.lOOkO.186 1.818kO.213

2.004-to.149 1.932kO.174

1.505-1-0.075 1.448z!zO.127

2.34520.252 2.115kO.247

2.296zk0.246 2.324kO.242

-0.063zkO.083 -0.066t0.068

-0.212+0.091 -0.225zkO.068

Lactate

. .

Placebo Treatment Venous Placebo Treatment Arteriovenous Placebo Treatment

TREATMENT

-0.292AO.210 -0.39lt0.134

Pyruvate Arterial Placebo Treatment Venous Placebo Treatment Arteriovenous Placebo Treatment Values are means evaluation.

PLACEBO

concentrations

TABLE

0.034~0.004 0.028AO.002

0.051zk0.004 0.042zkO.004

0.06OkO.005 0.056AO.007

0.027kO.002 0.024-+0.002

0.080~0.011 0.055~0.007

0.075kO.008 0.068z!z0.010

0.007~0.003

-0.031kO.008

-0.017+0.008

0.004t0.001

-0.014t0.007

-0.012~0.004

t SE in mmol/l;

n = 10 at all intervals

of

4. O2 and CO2 content

of arteriovenous blood in whole arm Rest

REST

60

MIN

* *p4.05

EXHAUSTION

vs

placebo

(MO)

FIG. 2. Fractional extraction of glucose across 1 arm at rest, after 60 min of exercise, and at exhaustion in subjects performing arm exercise. Percent extraction of glucose was determined by dividing arteriovenous concentration of glucose by arterial concentration of glucose. Values are means k SE.

02, ml/l00 ml Placebo Treatment COz, ml/l00 ml Placebo Treatment

60 min

8.46kl.08 7.87zk0.77 -7.44kO.95 -6.67kO.61

Exhaustion

9.69kO.79 ll.lOIkl.34

-10.01~1.20 -11.16-r-1.33

RQ

7.18kO.76 8.69kO.80 -7.24kl.12 -8.81dz1.14

Placebo 0.88kO.09 1.03zko.15 1.01,t0.11 Treatment 0.85kO.07 1.00~0.07 1.01~0.07 Values are means k SE; n = 10 at all intervals of evaluation. RQ, respiratory quotient (C02/02).

TABLE

5. Fuel substrate concentration Rest

in venuus blued 60 min

Exhaustion

Glycerol, pmol/ml

treatment compared with the placebo trial. Differences Placebo 1.13zkO.23 1.4620.20 1.8120.24 were not noted at exercise termination. Whole arm fracTreatment 0.87kO.23 0.95kO.17 1.62ztO.26 ,8-Hydroxybutyrate, pmol/ml tional glucose extraction (Fig. 2) was greater (P < 0.05) Placebo O.llkO.02 0.12zkO.02 0.63kO.23 before exercise, after 60 min of exercise, and at exhausTreatment 0.09+0.02 0.12kO.07 0.68&O. 15 tion during the treatment compared with the placebo FFA, meq/l trial. Arterial and venous lactate and pyruvate concenPlacebo 0.45AO.05 0.5OkO.07 1.83k0.38 Treatment 0.38kO.05 0.48kO.06 2.07kO.55 trations (Table 3) were not different across trials at any measurement period. Values are means 2 SE; n = 6 at all intervals of evaluation. FFA, Whole arm arteriovenous difference for 02 and COz free fatty acids. content and calculated RQ are presented in Table 4. Arteriovenous O2 and CO2 difference and RQ did not trials are presented in Table 5. Differences were not differ between trials before, after 60 min of exercise, or found between experimental trials at rest, after 60 min at termination of exercise. R at 1, 4, 10, and 60 min, of exercise, and at exhaustion for any of these variables. respectively, was 0.83 t 0.03, 1.03 t 0.03, 1.05 2 0.03, Arteriovenous differences for these fuel substrates also and 1.02 t 0.05 after consumption of placebo and 0.82 t did not differ between trials (data not presented). 0.05, 0.89 t 0.09, 1.01 k 0.01, and 1.02 t 0.02 after Plasma hormone concentrations for both experimental consumption of DHAP (P = NS at all times). trials are included in Table 6. Catecholamine and insulin Venous concentration of free fatty acids, P-hydroxyconcentrations did not differ between dietary treatments butyrate, and glycerol before and during the exercise at any measurement period. Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.108.009.184) on October 30, 2018. Copyright © 1990 American Physiological Society. All rights reserved.

EXERCISE

TABLE 6. Hormone

concentration

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123

in venous blood

increased with DHAP feeding in the present study. This finding suggests that the effect of DHAP on muscle Rest 60 min Exhaustion fractional utilization of glucose during exercise may be related to the effects of DHAP on muscle, liver, or both, Epinephrine, pg/ml 110t22 Placebo 49&6 119t19 but the mechanism at present is unknown. Treatment 83k12 104&10 146t30 The ergogenic effect of dietary DHAP supplementaNorepinephrine, pg/ml tion may also be linked to the comparatively greater Placebo 365-t-54 747t133 717t109 preexercise muscle glycogen content that was observed Treatment 257k40 7152154 87lk150 Insulin, pU/ml in the treatment trial. If the rate of muscle glycogen Placebo 7.7k2.7 6.7t1.9 5.1t1.9 depletion was the same in both trials, additional glycogen Treatment 9.9k3.7 3.2kO.4 5.6t1.6 would have been available during the later part of the Values are means t SE; IZ = 6 at all intervals of evaluation. exercise performance. This added source of CHO may have accounted for the longer endurance performance in DISCUSSION the DHAP trial. Because venous catecholamine and insulin concentraThe effect of dietary DHAP supplementation on blood tion were similar after feeding of the placebo and treatglucose extraction, muscle glycogen content, and sub- ment diets, changes in these hormone concentrations maximal arm endurance capacity was determined for 10 probably cannot explain the marked increases in muscle healthy young men. Consumption of DHAP as a portion glucose extraction at rest and during exercise in the of a regular diet for 1 wk increased arm exercise endurDHAP condition. ance capacity by 20%. After feeding DHAP for 1 wk, Subjects ingested daily doses of 25 g of pyruvate and whole arm arteriovenous glucose difference and frac- 75 g of dihydroxyacetone for 7 days before exercise tional extraction of glucose were increased postabsorptesting, but arterial and venous concentrations of lactate tively. Greater muscle arteriovenous glucose difference and pyruvate were similar to those seen with feeding of and fractional extraction of glucose after consumption of the glucose polymer. Studies of stool calorie content and DHAP persisted during exercise. In addition, triceps weight in rats (21) and human subjects (placebo, 0.59 t muscle glycogen concentration also increased with feed- 0.03 kcal/g wet wt; treatment, 0.65 t 0.04 kcal/g wet wt; ing of DHAP. This later finding is consistent with our P = NS; unpublished data) fed these metabolites suggest previous report of increased carcass glycogen concentraDHAP is not malabsorbed. It would seem that on feeding tion in rats after dietary supplementation of DHAP (21). DHAP is immediately absorbed. The present findings suggest that dietary consumption A fivefold increase in arteriovenous glucose concentraof DHAP over a 7-day period increased glucose availability to muscle, thereby prolonging submaximal arm tion has been reported (1) in subjects performing arm exercise at 30% VOzpeak.In the present study, an identical endurance exercise. Both arteriovenous glucose difference and fractional glucose extraction were greater in increase in glucose extraction (arteriovenous difference) across the whole arm occurred during exercise after the DHAP trials. Although CHO metabolism was not feeding of the placebo (i.e., glucose polymer). Concerning measured directly, these responses suggest augmented DHAP feeding, the greatest effect on muscle glucose uptake and oxidation of glucose by exercising muscle extraction was seen at rest. Muscle glucose extraction with DHAP. R and RQ did not differ between trials, and increased only 60% with exercise after consumption of both values were ~1. This negates their use in determinDHAP. This attenuated increase may be partially exing differential substrate oxidation. As such, the mechplained by the large glucose extraction at rest. Actually, anism regarding the pathway for CHO metabolism after glucose extraction at rest (0.60 t 0.12 mmol/l) after DHAP supplementation remains speculative. NevertheDHAP ingestion was similar to the extraction after exless, these findings are compatible with the concept of ercise termination (i.e., exhaustion) in the placebo conprolonged glucose oxidation and extended endurance performance in the DHAP group. It is of note that the dition. Ahlborg et al. (1) report a similar arteriovenous comparatively high R and RQ obtained for arm exercise glucose difference (0.67 t 0.13 mmol/l) after 2 h of arm at an intensity equivalent to 60% Vozpeak would not be exercise in subjects fed a regular diet resembling the placebo diet used presently. Stimuli for glucose extracexpected for leg exercise at the same relative metabolic rate. However, because the present subjects were not tion by muscle were as active at rest in our treated specifically trained for arm exercise, it is likely that the subjects as that induced by prolonged exhaustive exercise blood lactate inflection point was ~60% VOWpeak (5). in subjects fed a regular diet. Blood flow at rest was 135 t 2 ml/min after the placebo Therefore, prolonged exercise at this intensity may have diet and 135 t 5 ml/min after the treatment diet. Because required modest buffering of metabolic acidosis, causing blood flow was similar after the placebo and treatment a comparatively high R and RQ. diets, increases in arteriovenous glucose differences after A recent study on rats (22) suggests that hepatic consumption of DHAP probably represent actual inglycogenolysis and glucose release during submaximal creases in glucose extraction from blood by muscle. Irexercise are directly related to hepatic glycogen content. Although studies in our laboratory show that feeding of respective of blood flow, fractional extraction of glucose DHAP to rats increases carcass glycogen (21) and causes was increased before and after 60 min of exercise and at exhaustion. Porter et al. (18) report a resting blood flow a twofold increase in hepatic glycogen content (unpublished data), arterial glucose (hepatic release) was not for the forearm of 149 ml/min in subjects ~50 yr of age. Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.108.009.184) on October 30, 2018. Copyright © 1990 American Physiological Society. All rights reserved.

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With exercise for 60 min blood flow was 324 t 20 ml/ min after the placebo diet and 322 t 24 ml/min after the treatment diet. Although resistivity of blood may vary with viscosity (14), hematocrit changes with exercise were similar after both diets. Therefore, comparison of blood flow between trials was considered valid. The indirect electrical impedance technique has only been validated by comparison with cardiac output dye techniques during rest and exercise (6), but the nearly identical values for blood flow at rest and during exercise after feeding of the two diets in the present study would suggest that blood flow would probably not differentially affect the metabolic parameters investigated. The proportion of energy derived from lipolysis during exercise was not influenced by dietary DHAP supplementation. Ven .ous concentrations of glycerol, p -hydroxybutyrate, and free fatty acids were the same between the DHAP and placebo trials. As such, augmented sources of CHO rather than fat presumably accounted for the prolongation of endurance exercise in the DHAP trial. These findings also provide indirect evidence that dietary supplementation of DHAP does not impair free fatty acid mobilization during prolonged submaximal exercise. Feeding of DHAP induced few obvious side effects. Borborygmus and flatus occurred in most subjects with consumption of the treatment diet. Biochemical profile and blood count were normal in all subjects after both dietary protocols. One subject developed dizziness after feeding of DHAP and could not complete an exercise trial. Data from this subject are not presented. One subject’s endurance capacity (Tables 1 and 7) was lower after feeding of DHAP than the glucose polymer. Individual response to ingestion of high concentrations (i.e., 400 kcal/day) of DHAP probably will occur with variable effects. Previous studies have shown that exercise endurance capacity can be enhanced with glucose supplementation (3, 4) and carbohydrate supercompensation (2, 13, 20). The present study indicates that endurance capacity of arms during submaximal exercise can also be increased by adding DHAP to a standard diet for 7 days. We conclude that feeding of DHAP increases arm muscle glucose extraction at rest and during exercise, thereby enhancing endurance capacity.

3. 4.

5. 6.

7. 8. 9. 10. 11. 12. 13. 14.

15. 16. 17. 18. 19.

20.

We thank Judith E. Arch. We also thank Robert H. Miller and Arthur L. Hecker (Ross Laboratories) for assistance. Address for reprint requests: R. T. Stanko, Montefiore Hospital, 3459 Fifth Ave., Pittsburgh, PA 15213.

21.

Received 3 January 1989; accepted in final form 30 August 1989.

22.

REFERENCES

23.

1. AHLBORG, G., J, WAHREN, AND P. FELIG. Splanchnic and peripheral glucose and lactate metabolism during and after prolonged arm exercise. J. CLin. Inuest. 77: 690-699, 1986. 2. BERGSTROM, J., L. HERMANSEN, E. HULTMAN, AND B. SALTIN.

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